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In vivo radioadaptive response: A review of studies relevant to radiation-induced cancer risk
https://repo.qst.go.jp/records/58453
https://repo.qst.go.jp/records/58453c5a940ff-8838-4e09-b714-c1d1d11bbc91
| Item type | 一般雑誌記事 / Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2014-06-19 | |||||
| タイトル | ||||||
| タイトル | In vivo radioadaptive response: A review of studies relevant to radiation-induced cancer risk | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
根井, 充
× 根井, 充× 王, 冰× Ｇｕｉｌｌａｕｍｅ, Ｖａｒｅｓ× 根井 充× 王 冰× Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Radioadaptive response (RAR) describes phenomena where small conditioning doses of ionizing radiation (IR) reduce detrimental effects of subsequent higher IR doses. Current radiation protection regulations do not include RAR because of the large variability in expression among individuals and uncertainties of the mechanism. However, RAR should be regarded as an indispensable factor for estimation and control of individual IR sensitivity. In this article, RAR studies relevant to individual cancer risk are reviewed. Using various strains of mice, carcinogenic RAR has been demonstrated. Consistently much in vivo evidence for RAR with end points of DNA and chromosome damage is reported. Most in vivo RAR studies revealed efficient induction of RAR by chronic or repeated low-dose priming irradiation. Chronic IR-induced RAR was observed also in human individuals after environmental, occupational, and nuclear accident radiation exposure. These observations may be associated with an intrinsically distinct feature of in vivo experimental systems that mainly consist of nonproliferationg mature cells. Alternatively, induction of RAR by gap junction-mediated bystander effects suggests that multicellular systems comprising densely communicating cells may be capable of responding to long-lasting low-dose-rate priming irradiation. Regulation by endocrine factors is also a plausible mechanism for RAR at an individual level. Emerging evidence suggests that glucocorticoids, known as stress hormones, participate in in vivo RAR induction following long-term low-dose-rate exposure to IR. | |||||
| 書誌情報 |
Human and Experimental Toxicology p. 1-12, 発行日 2014-06 |
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